Abstract
In this issue of the European Journal of Cardio-Thoracic Surgery, Xue et al. [1] describe an experimental study in isolated rat hearts that examines the cardioprotective efficacy of 3 clinical cardioplegia solutions: an extracellular-type K+-based dilute blood solution [del Nido cardioplegia (DNC)], an intracellular-type crystalloid solution [Bretschneider histidine-tryptophan-ketoglutarate cardioplegia (HTK)] and a combination of a blood cardioplegia [Buckberg (BC)] and HTK, with outcomes measured in terms of myocardial or endothelial protection. The study was conducted to determine the efficacy of the combined approach (BC + HTK) that is used clinically by these authors (with stated excellent results). The rationale for this combined approach was their clinical observation that the intracellular HTK solution was relatively slower to induce cardiac arrest than that achieved with the elevated potassium-based extracellular solutions; hence, they used the potassium-based cardioplegia to induce arrest and then HTK to maintain the arrest for a longer period. Clinically, HTK solution is used with a high volume infused over a longer period than that of potassium-based cardioplegia; in the experimental study, HTK was infused at the same rate as DNC. It was shown that DNC provided the best haemodynamic recovery, whereas HTK and BC + HTK provided optimal endothelial protection. The concept of confirming the efficacy of a clinical scenario is unusual; it is more usual to conduct the experimental research prior to initiating clinical confirmation. One wonders what the authors would have done in their patients if their clinical scenario had proved less efficacious in the experimental study! They concluded that no solution provides optimal protection so warranting more research in this area.
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